VEGF‐A, VEGF‐D and VEGF‐D<sup>ΔNΔC</sup> induced intimal hyperplasia in carotid arteries

Bhardwaj, Shalini; Roy, Himadri; Heikura, Tommi; Ylä‐Herttuala, Seppo

doi:10.1111/j.1365-2362.2005.01555.x

Cited by 76 publications

(69 citation statements)

References 23 publications

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“…This is in line with the suggestion that adventitial angiogenesis contributes to atherosclerotic plaque growth because the degree of adventitial angiogenesis correlates with the extend of neointima formation. 21,22 In addition, stimulation of adventitial angiogenesis, by administration of endothelial progenitor cells or adventitial application of VEGF, results in increased neointima formation. 23,24 Recently, circulating hematopoietic stem cells were shown to differentiate into vascular cells that participate in atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Vaccination Against VEGFR2 Attenuates Initiation and Progression of Atherosclerosis

Hauer

Puijvelde

Peterse

et al. 2007

ATVB

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Objective-Vascular endothelial growth factor receptor 2 (VEGFR2)-overexpressing cells may form an interesting target for the treatment of atherosclerosis because of their involvement in processes that contribute to this disease, such as angiogenesis. Methods and Results-We vaccinated mice against VEGFR2 by an orally administered DNA vaccine, comprising a plasmid, encoding murine VEGFR2, carried by live attenuated Salmonella typhimurium. This vaccine induces cellular immunity against cells that overexpress VEGFR2. Vaccination of hypercholesterolemic mice against VEGFR2 resulted in a marked induction of CD8 ϩ cytotoxic T cells specific for VEGFR2 and led to an inhibition of angiogenesis in a hindlimb ischemia model. Interestingly, VEGFR2 vaccination attenuated the progression of preexisting advanced atherosclerotic lesions in the brachiocephalic artery of apoE Ϫ/Ϫ mice. Furthermore, VEGFR2 vaccination strongly reduced the initiation of collar-induced atherosclerosis in the carotid arteries of LDLr Ϫ/Ϫ mice. In addition, denudation of the carotid artery, as a model for postinterventional lesion formation, resulted in delayed endothelial replacement and significantly increased neointima formation on VEGFR2 vaccination. Conclusions-These data indicate the prominent role of VEGFR2ϩ cells in cardiovascular diseases and show that induction of cellular immunity against atherosclerosis-associated cells by means of DNA vaccination may contribute to the development of novel therapies against atherosclerosis. (Arterioscler Thromb Vasc

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Section: Discussionmentioning

confidence: 99%

Vaccination Against VEGFR2 Attenuates Initiation and Progression of Atherosclerosis

Hauer

Puijvelde

Peterse

et al. 2007

ATVB

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“…For example, local gene transfer of VEGF-A significantly increases intimal hyperplasia after balloon injury 49 or application of silastic collars. 52 Intraluminal infusion of VEGF-A to denuded rat carotid arteries doubled the mitogenic response to infused FGF-2 by increasing intimal SMC replication. 24 Moreover, systemic delivery of soluble Flt1 (which blocks VEGF-A-VEGFR1/Flt1 binding) attenuated neointima formation after balloon injury without affecting luminal reendothelialization.…”

Section: Malabanan Et Al Atf-4 Controls Vegf-a and Neointima Formationmentioning

confidence: 99%

Activation Transcription Factor-4 Induced by Fibroblast Growth Factor-2 Regulates Vascular Endothelial Growth Factor-A Transcription in Vascular Smooth Muscle Cells and Mediates Intimal Thickening in Rat Arteries Following Balloon Injury

Malabanan

Kanellakis

Bobik

et al. 2008

Circulation Research

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Abstract-Activation transcription factor (ATF)-4 is a member of the ATF/CREB family of basic leucine zipper transcription factors that regulates cellular responses to a variety of stresses. The role of ATF-4 in smooth muscle cells of the vessel wall is completely unknown. Here, we show that ATF-4 expression is induced in smooth muscle cells in response to injury, both in vitro using a model of mechanical injury and in the media of balloon-injured rat carotid arteries. We demonstrate that ATF-4 is activated by fibroblast growth factor (FGF)-2, an injury-induced mitogen, through the phosphatidylinositol 3-kinase pathway. Injury also activates vascular endothelial growth factor (VEGF) -

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“…33 Similarly, adenoviral gene transfer of VEGF-A and VEGF-D to adventitia induced robust adventitial angiogenesis, whereas VEGF-B adenoviral gene transfer failed to do so. 34,45 Another study also showed that VEGF-B 167 gene delivery to the skin or ischemic limb did not induce blood vessel growth. 10 Furthermore, VEGF-B 167 recombinant protein injection into mouse eyes at a dose effective for retinal neuron survival did not induce ocular angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

Vegf-B

Lee

Tang

et al. 2009

Cell Adhesion & Migration

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Despite its early discovery and high sequence homology to the other VEGF family members, the biological function of VEGF-B remained debatable for a long time, and VEGF-B has received little attention from the field thus far. Recently, we and others have found that (1) VEGF-B is a potent survival factor for different types of cells by inhibiting apoptosis via suppressing the expression of BH3-only protein and other apoptotic/cell deathrelated genes. (2) VEGF-B has a negligible role in inducing blood vessel growth in most organs. Instead, it is critically required for blood vessel survival. VEGF-B targeting inhibited pathological angiogenesis by abolishing blood vessel survival in different animal models. (3) Using different types of neuro-injury and neurodegenerative disease models, VEGF-B treatment protected endangered neurons from apoptosis without inducing undesired blood vessel growth or permeability. Thus, VEGF-B is the first member of the VEGF family that has a potent survival/antiapoptotic effect, while lacking a general angiogenic activity. Our work thus advocates that the major function of VEGF-B is to act as a "survival," rather than an "angiogenic" factor and implicates a therapeutic potential of VEGF-B in treating different types of vascular and neurodegenerative diseases.

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VEGF‐A, VEGF‐D and VEGF‐D^ΔNΔC induced intimal hyperplasia in carotid arteries

Cited by 76 publications

References 23 publications

Vaccination Against VEGFR2 Attenuates Initiation and Progression of Atherosclerosis

Vaccination Against VEGFR2 Attenuates Initiation and Progression of Atherosclerosis

Activation Transcription Factor-4 Induced by Fibroblast Growth Factor-2 Regulates Vascular Endothelial Growth Factor-A Transcription in Vascular Smooth Muscle Cells and Mediates Intimal Thickening in Rat Arteries Following Balloon Injury

Vegf-B

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VEGF‐A, VEGF‐D and VEGF‐DΔNΔC induced intimal hyperplasia in carotid arteries

Cited by 76 publications

References 23 publications

Vaccination Against VEGFR2 Attenuates Initiation and Progression of Atherosclerosis

Vaccination Against VEGFR2 Attenuates Initiation and Progression of Atherosclerosis

Activation Transcription Factor-4 Induced by Fibroblast Growth Factor-2 Regulates Vascular Endothelial Growth Factor-A Transcription in Vascular Smooth Muscle Cells and Mediates Intimal Thickening in Rat Arteries Following Balloon Injury

Vegf-B

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VEGF‐A, VEGF‐D and VEGF‐D^ΔNΔC induced intimal hyperplasia in carotid arteries